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Expression of minor cartilage collagens and small leucine rich proteoglycans may be relatively reduced in osteoarthritic cartilage.
Tanaka, Nobuho; Tashiro, Toshiyuki; Katsuragawa, Yozo; Sawabe, Motoji; Furukawa, Hiroshi; Fukui, Naoshi.
Afiliación
  • Tanaka N; Clinical Research Center, National Hospital Organization Sagamihara Hospital, 18-1 Sakuradai, Sagamihara, Kanagawa, 252-0315, Japan.
  • Tashiro T; Department of Orthopaedic Surgery, Tokyo Yamate Medical Center, 3-22-1 Hyakuninncyou, Shinjyuku-ku, Tokyo, 169-0073, Japan.
  • Katsuragawa Y; Department of Orthopaedic Surgery, Center Hospital of the National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjyuku-ku, Tokyo, 162-8655, Japan.
  • Sawabe M; Department of Molecular Pathology, Graduate School of Health Care Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
  • Furukawa H; Laboratory for Molecular and Genetic Epidemiology, School of Medicine, The University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
  • Fukui N; Clinical Research Center, National Hospital Organization Sagamihara Hospital, 18-1 Sakuradai, Sagamihara, Kanagawa, 252-0315, Japan. n-fukui@idaten.c.u-tokyo.ac.jp.
BMC Musculoskelet Disord ; 20(1): 232, 2019 May 18.
Article en En | MEDLINE | ID: mdl-31103042
ABSTRACT

BACKGROUND:

In osteoarthritis (OA), cartilage matrix is lost despite vigorous chondrocyte anabolism. In this study, we attempted to determine whether altered matrix synthesis is involved in this paradox in disease progression through gene expression analysis and ultrastructural analysis of collagen fibrils within the cartilage matrix.

METHODS:

Cartilage tissues were obtained from 29 end-stage OA knees and 11 control knees. First, cDNA microarray analysis was performed and the expression of 9 genes involved in collagen fibrillogenesis was compared between OA and control cartilages. Then their expression was investigated in further detail by a quantitative polymerase chain reaction (qPCR) analysis combined with laser capture microdissection. Finally, collagen fibril formation was compared between OA and control cartilage by transmission electron microscopy.

RESULTS:

The result of the microarray analysis suggested that the expression of type IX and type XI collagens and fibrillogenesis-related small leucine-rich proteoglycans (SLRPs) may be reduced in OA cartilage relative to the type II collagen expression. The qPCR analysis confirmed these results and further indicated that the relative reduction in the minor collagen and SLRP expression may be more obvious in degenerated areas of OA cartilage. An ultrastructural analysis suggested that thicker collagen fibrils may be formed by OA chondrocytes possibly through reduction in the minor collagen and SLRP expression.

CONCLUSIONS:

This may be the first study to report the possibility of altered collagen fibrillogenesis in OA cartilage. Disturbance in collagen fibril formation may be a previously unidentified mechanism underlying the loss of cartilage matrix in OA.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Cartílago Articular / Osteoartritis de la Rodilla / Colágeno Tipo XI / Colágeno Tipo IX / Proteoglicanos Pequeños Ricos en Leucina Límite: Aged / Aged80 / Humans Idioma: En Revista: BMC Musculoskelet Disord Asunto de la revista: FISIOLOGIA / ORTOPEDIA Año: 2019 Tipo del documento: Article País de afiliación: Japón

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Cartílago Articular / Osteoartritis de la Rodilla / Colágeno Tipo XI / Colágeno Tipo IX / Proteoglicanos Pequeños Ricos en Leucina Límite: Aged / Aged80 / Humans Idioma: En Revista: BMC Musculoskelet Disord Asunto de la revista: FISIOLOGIA / ORTOPEDIA Año: 2019 Tipo del documento: Article País de afiliación: Japón